Photoenhanced transformation of hydroxylated fullerene (fullerol) by free chlorine in water

2017 ◽  
Vol 4 (2) ◽  
pp. 470-479 ◽  
Author(s):  
Jiewei Wu ◽  
Lawrence B. Alemany ◽  
Wenlu Li ◽  
Denise Benoit ◽  
John D. Fortner

Water-soluble, oxidized fullerenes, termed as fullerols or fullerenols, have gained increasing attention as they have been identified as primary daughter product(s) when C60 is exposed to ubiquitous, reactive (oxidative) environmental scenarios including UV light (including sunlight UVA), radical oxygen species (ROS), and ozone.

2020 ◽  
Vol 90 (5-6) ◽  
pp. 439-447 ◽  
Author(s):  
Andrew Hadinata Lie ◽  
Maria V Chandra-Hioe ◽  
Jayashree Arcot

Abstract. The stability of B12 vitamers is affected by interaction with other water-soluble vitamins, UV light, heat, and pH. This study compared the degradation losses in cyanocobalamin, hydroxocobalamin and methylcobalamin due to the physicochemical exposure before and after the addition of sorbitol. The degradation losses of cyanocobalamin in the presence of increasing concentrations of thiamin and niacin ranged between 6%-13% and added sorbitol significantly prevented the loss of cyanocobalamin (p<0.05). Hydroxocobalamin and methylcobalamin exhibited degradation losses ranging from 24%–26% and 48%–76%, respectively; added sorbitol significantly minimised the loss to 10% and 20%, respectively (p < 0.05). Methylcobalamin was the most susceptible to degradation when co-existing with ascorbic acid, followed by hydroxocobalamin and cyanocobalamin. The presence of ascorbic acid caused the greatest degradation loss in methylcobalamin (70%-76%), which was minimised to 16% with added sorbitol (p < 0.05). Heat exposure (100 °C, 60 minutes) caused a greater loss of cyanocobalamin (38%) than UV exposure (4%). However, degradation losses in hydroxocobalamin and methylcobalamin due to UV and heat exposures were comparable (>30%). At pH 3, methylcobalamin was the most unstable showing 79% degradation loss, which was down to 12% after sorbitol was added (p < 0.05). The losses of cyanocobalamin at pH 3 and pH 9 (~15%) were prevented by adding sorbitol. Addition of sorbitol to hydroxocobalamin at pH 3 and pH 9 reduced the loss by only 6%. The results showed that cyanocobalamin was the most stable, followed by hydroxocobalamin and methylcobalamin. Added sorbitol was sufficient to significantly enhance the stability of cobalamins against degradative agents and conditions.


2013 ◽  
Vol 142-143 ◽  
pp. 662-667 ◽  
Author(s):  
Luis Domínguez Sánchez ◽  
Sébastien Francis Michel Taxt-Lamolle ◽  
Eli Olaug Hole ◽  
André Krivokapić ◽  
Einar Sagstuen ◽  
...  

2018 ◽  
Vol 22 (08) ◽  
pp. 686-692 ◽  
Author(s):  
Armağan Günsel ◽  
Hatice Tunca ◽  
Ahmet T. Bilgiçli ◽  
Ali Doğru ◽  
M. Nilüfer Yaraşir ◽  
...  

In this study, we have analyzed the effect a newly synthesized water-soluble alpha tetra-substituted zinc phthalocyanine (Pc) compound on superoxide dismutase (SOD), ascorbate peroxidase (APX) and glutathione reductase (GR) activities and biomass accumulation in the Arthrospira platensis-M2 strain to test whether this compound could be used as an algaecide or not. We found that lower concentrations (3 μg mL[Formula: see text] and 6 μg mL[Formula: see text] of Pc compound were not toxic to algae cells, as indicated by enduring biomass accumulation during the study (7 days). Higher Pc concentrations, however, were toxic and inhibited biomass accumulation. This inhibition appeared on the fourth day and persisted during the study. At higher Pc concentrations, SOD activity decreased significantly, but APX and GR activity were not affected. These results may show that Pc applications did not cause the accumulation of reactive oxygen species in Arthrospira platensis-M2 cells. Our result suggests that higher Pc concentrations did not cause oxidative stress but biomass accumulation inhibited, possibly due to some different toxicity mechanism(s), which should be carried out in the future studies. As a result, we may offer use of this compound as a means to keep under control algal populations in natural environments.


2018 ◽  
Vol 51 (3) ◽  
pp. 1287-1300 ◽  
Author(s):  
Manel Vera ◽  
Sergi Torramade-Moix ◽  
Susana Martin-Rodriguez ◽  
Aleix Cases ◽  
Josep M. Cruzado ◽  
...  

Background/Aims: Accelerated atherosclerosis in chronic kidney disease (CKD) is preceded by endothelial dysfunction (ED), which exhibits a proinflammatory and prothrombotic phenotype and enhanced oxidative stress. In this study, the effect of several compounds with anti-inflammatory and/or antioxidant properties on uremia-induced endothelial dysfunction has been evaluated in an in vitro model. Methods: Endothelial cells (ECs) were exposed to sera from uremic patients in the absence and presence of the flavonoids apigenin, genistein and quercetin, the antioxidant enzyme mimetics (AEM) ebselen (glutathione peroxidase mimetic), EUK-134 and EUK-118 (both superoxide dismutase mimetics), and the pharmacological drug N-acetylcysteine (NAC). We explored changes in the expression of adhesion receptors on the cell surface, by immunofluorescence, the production of radical oxygen species (ROS), by fluorescence detection, and the activation of signaling proteins related to inflammation, by both a phosphospecific antibody cell-based ELISA and immunoblotting techniques. Results: Uremic media induced a significantly increased expression of ICAM-1, overproduction of radical oxygen species (ROS) and activation of p38 mitogen activated protein kinase (p38MAPK) and Nuclear Factor kB (NFkB) in ECs. Quercetin, the AEM and NAC showed a significant inhibitory effect on both ICAM-1 expression and ROS generation (p<0.05). All the compounds reduced p38MAPK activation, but only the AEM, especially ebselen, and NAC, both potentiating the glutathione peroxidase pathway, also inhibited NFkB activation. These two compounds were capable of increasing endothelial glutathione levels, especially in response to uremia. Conclusion: Our results indicate that the potentiation of the antioxidant pathways can be an effective strategy to improve endothelial dysfunction in uremia and a potential target to reduce the cardiovascular risk in this population.


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